Cytokines regulate complement receptor immunoglobulin expression and phagocytosis of Candida albicans in human macrophages: A control point in anti-microbial immunity

Usma Munawara, Annabelle Small, Alex Quach, Nick Gorgani, Catherine Abbott, Antonio Ferrante

    Research output: Contribution to journalArticlepeer-review

    7 Citations (Scopus)

    Abstract

    Complement Receptor Immunoglobulin (CRIg), selectively expressed by macrophages, plays an important role in innate immunity by promoting phagocytosis of bacteria. Thus modulation of CRIg on macrophages by cytokines can be an important mechanism by which cytokines regulate anti-microbial immunity. The effects of the cytokines, tumor necrosis factor, transforming growth factor-β1, interferon-Î 3, interleukin (IL)-4, IL-13, IL-10, IL-1β, IL-6, lymphotoxin-α, macrophage-colony stimulating factor (M-CSF) and GM-CSF on CRIg expression were examined in human macrophages. We demonstrated that cytokines regulated the CRIg expression on macrophages during their development from monocytes in culture at the transcriptional level using qPCR and protein by Western blotting. Both CRIg spliced forms (Long and Short), were similarly regulated by cytokines. Direct addition of cytokines to matured CRIg+ macrophages also changed CRIg mRNA expression, suggesting that cytokines control macrophage function via CRIg, at two checkpoints. Interestingly the classical complement receptors, CR3 and CR4 were differentially regulated by cytokines. The changes in CRIg but not CR3/CR4 mRNA expression correlated with ability to phagocytose Candida albicans by macrophages. These findings suggest that CRIg is likely to be a control point in infection and immunity through which cytokines can mediate their effects, and is differentially regulated from CR3 and CR4 by cytokines.

    Original languageEnglish
    Article number4050
    Pages (from-to)Art: 4050
    Number of pages16
    JournalScientific Reports
    Volume7
    Issue number1
    DOIs
    Publication statusPublished - 22 Jun 2017

    Bibliographical note

    Publisher Copyright:
    © 2017 The Author(s).

    Copyright:
    Copyright 2017 Elsevier B.V., All rights reserved.

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